Now, a multidisciplinary research team led by David Eckmann, MD, PhD, Horatio C. Wood Professor of Anesthesiology and Critical Care at the Perelman School of Medicine at the University of Pennsylvania and professor of Bioengineering in Penn's School of Engineering and Applied Science, has found that when delivered by a microscopic transporter called a nanocarrier, steroids can access the hard - to - reach
lung endothelial cells that need it most and are successful at preventing inflammation in mice.
A specific lung - targeting molecule is attached to the carrier's surface and the steriod, dexamethasone, an anti-inflammatory, is loaded into the nanogel, which then binds to
lung endothelial cells lining the inside wall of the blood vessels where it rapidly delivers the drug.
By blocking these in
lung endothelial cells, the researchers were able to slow lung tumor growth in mice and also reduce the spread of metastatic tumors.
The best results were seen in
lung endothelial cells, but the particles also successfully delivered RNA to the kidneys and heart, among other organs.
In experiments conducted on human
lung endothelial cells and in mice, the researchers showed that NS1 caused permeability of the endothelium, which lines the walls of blood and lymph vessels.
Not exact matches
A team from Cold Spring Harbor Laboratory in Long Island, N.Y., reports that it staved off full - blown metastasis in mice by preventing mini-tumors in the
lungs from recruiting stem
cells called
endothelial progenitors, which assemble into blood vessels to nourish the malignancy.
To determine whether
endothelial cells — the
cells that line the interior surface of blood vessels — directly influence breast cancer
cell growth, they then created unique organotypic models of
lung and bone marrow microvascular niches, in which
endothelial cells formed blood vessel - like structures in culture as they would in the original organ.
The study examined nanoparticle entry into
endothelial cells and macrophages for the in vitro study, and the same type of
cells from the
lung, heart and bone marrow for the in vivo component.
This experiment uses quantitative PCR to detect the expression level of POSTN in CD34 + / CD31 − pulmonary fibroblasts, CD31 +
endothelial cells, and CD45 + immune
cells isolated from
lungs of mice with macrometastases, which is a replication of the experiment reported in Figure 2H.
Cultured
endothelial cells from
lung, colon, kidney, bladder, liver, and ovary displayed a cobblestone appearance after reaching confluence.
Additionally, ERCs were reported to be able to differentiate into, or become,
cells from the three different germ layers (see the previous post on MSCs for more details): mesoderm (muscle, bone, fat, cartilage, and
endothelial cells), ectoderm (neurons), and endoderm (liver, pancreas, and
lung cells)(Meng et al., 2007; Patel et al., 2008).
Organ - on - a-chip technology may in part overcome this limitation, as exemplified by the «breathing»
lung - on - a-chip that recapitulates the alveolar - capillary interface by co-culturing human alveolar epithelial
cells and capillary
endothelial cells on opposite sides of a flexible, porous, ECM - coated membrane.
Embryonic
endothelial progenitor
cells armed with a suicide gene target hypoxic
lung metastases after intravenous delivery.
To assess the expression of Tie2 and other Ang / Tie signalling molecules on human pericytes, a microarray - based expression profiling of human brain pericytes (BP), placenta pericytes, pancreas pericytes (PA),
lung pericytes (LP), muscle pericytes (MP) and human umbilical vein
endothelial cells (HUVEC) was performed.
Phase II study of cediranib (AZD 2171), an inhibitor of the vascular
endothelial growth factor receptor, for second - line therapy of small
cell lung cancer (NCI # 7097).
â $ œWe have solved a major obstacle of using anti-miRNA as a therapeutic by being able to do a targeted delivery to only inflamed
endothelial cells while all other tissues examined, including liver,
lung, kidney, blood
cells, spleen, etc showed no detectable side - effects, â $ Jo says.
We demonstrate a novel outcome of S1P - mediated regulation of lymphocyte trafficking, whereby deletion of Spns2, either globally or in a lymphatic
endothelial - specific manner, creates a circulating lymphopenia and a higher percentage of effector T
cells and natural killer (NK)
cells present in the
lung.